BTF3 promotes stemness and inhibits TypeIInterferon signaling pathway in triple-negative breast cancer.

Abstract Triple-negative breast cancer (TNBC) is a major challenge in clinical practice due to its aggressiveness and lack of targeted treatment. Cancer stem-like traits contribute to tumorigenesis and immune privilege of TNBC. However, the relationship of stemness and immunosurveillance remains unclear. Here, we demonstrate that BTF3 expression is related with stem-like properties in TNBC cells. BTF3 modulates stemness, migration and proliferation of TNBC in vitro. Bioinformatics analysis revealed that interferon signaling pathways and IRF7, both of which participate in the immune escape of TNBC, are closely related to BTF3 in TNBC cells. Knockdown of BTF3 activates IRF7 expression through increased degradation of BMI1, a protein that can represses IRF7 transcription by directly binding to its promotor region. BTF3 links stem-like traits and the interferon signaling pathway, revealing the potential connection of stemness and immunomodulation in TNBC. Clinically, we suggest that BTF3 is predictive of poor prognosis in patients with TNBC. Together, our findings highlight an important role of BTF3 in regulating the progression of TNBC cells.